Thrombosis, an excessive formation of clot within a blood vessel, gives rise to thrombotic strokes, deep vein thrombosis, myocardial infarction and other medical conditions which may result in necrosis of tissues and oftentimes death of a patient. Even if death does not occur, thrombotic attacks are accompanied by damage to cells to which circulation has been prevented by thrombi formation. Removal of the thrombi by lysis is essential and the rate of lysis may be critical in ultimate patient recovery.
Lysis may occur normally in hours or days by the action of a proteolytic enzyme, plasmin, which is present in plasma as the inactive precursor, plasminogen, and which is activated by plasminogen activators, such as (pro)urokinase, urokinase or tissue plasminogen activator. Since the occurrence of a thrombotic event calls for rapid remedial action, administration of exogenous tissue plasminogen activator or (pro)urokinase is currently looked to in thrombolytic or fibrinolytic therapy. However, a still further reduction in lysis time is necessary to minimize cell injury.
Factor XIIIa is an enzyme responsible for the final event in the coagulation of blood. It is a plasma or platelet transglutaminase which is the activated form of Factor XIII, also known as fibrin-stabilizing-factor. It is essential for normal hemostasis and is responsible for the cross-linking of fibrin. This step is sometimes described as the transformation of soft clot to hard clot.